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Pharmacology Block 2 > Anesthetics > Flashcards

Anesthetics Flashcards

1
Q

Properties of general anesthetics

A
  • amnesia/unconsciousness
  • analgesia
  • blunting of reflexas
  • muscle relaxation
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2
Q

What do you use to induce amnesia

A

N2O, benzodiazepines

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3
Q

What do you use to induce analgesia

A

opoids

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4
Q

What do you use to blunt reflexes

A

GA’s, opoids

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5
Q

What do you use to relax muscle tone?

A

NMB’s

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6
Q

What are the two types of anesthetics?

A

Inhaled & Intravenous

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7
Q

Desflurane

A

-inhaled

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8
Q

Sevoflurane

A
  • inhaled

- (toxicity) can make CO with CO2 absorber– but not really anymore

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9
Q

Isoflurane

A

-inhaled

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10
Q

Enflurane

A
  • inhaled
  • not used clinically in US
  • (toxicity) Fluoride ion in this drug can cause renal failure
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11
Q

Halothane

A
  • inhaled
  • not used clinically in US
  • used in children scared of IV- overdose to get to brain quickly (6x MAC)
  • (toxicity) Can cause hepatitis in adults
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12
Q

Thiopental

A
  • IV

- Can’t be used for capital punishment

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13
Q

Etomidate

A
  • IV
  • Causes severe nausea and vomit
  • Used in hemodynamically unstable patients (CHF, trauma patients)
  • Doesn’t affect bp
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14
Q

Propofol

A
  • IV
  • Michael Jackson
  • Decr bp
  • Potent respiratory depressant
  • Can be used as a sole anesthetic agent– but you need very high doses
  • Can cause death
  • NO muscle relaxation (exception)
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15
Q

Ketamine

A
  • IV
  • induces anesthesia
  • dissociative
  • at low doses potent analgesic and dysphoria
  • dissociative anesthesia – takes away emotion component of pain (I’m in pain but I don’t know what that means)
  • Hallucinations
  • Potent sympathomimetic (CV stimulant)
  • Preserves airway reflexes
  • INCREASES cerebral blood flow
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16
Q

Methohexital

A

-IV

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17
Q

4 stages of inhalation anesthesia

A

1- Analgesia; airway reflexes intact, patient conscious.
-used to be used in labor and delivery
2- Excitement and disinhibition. We have reflex in glottis that causes vocal cords to close and cut off our airways (laryngospasm) –> can’t breathe. We avoid this stage.
3- Surgical anesthesia. Patient can still breathe and maintain some level of bp. Where we want to be.
4- Medullary center depression.

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18
Q

What part of the brain is most susceptible to anesthesia?

A

Cerebral cortex

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19
Q

3 goals of the anesthesiologist

A

1- Maintain homeostasis: O2 and ventilation, CO and bp, protect unconscious patient from injury
2-Provide optimal conditions for the surgeon; a still and bloodless field
3-perioperative care; optimize patient pre-,intra-, and post- operatively

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20
Q

Most common OR injury

A

Corneal abrasions

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21
Q

We measure inhalation anesthesia in terms of _____

A

partial pressure NOT concentration

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22
Q

Describe the the state (S,L,G) of the inhalation anesthetics and how we administer it.

A

volatile liquids with low boiling point- so administer them in a vaporizer as a gas along with a carrier gas (O2 in the air or NO2)

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23
Q

The ____ soluble a anesthetic in blood, the _____ more molecules are needed to achieve a given partial pressure

A

more, more

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24
Q

_____ (more/less) soluble agents produce _____(slower/faster) induction AND ______(slower/faster) recovery

A

Less, faster, faster

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25
Q

What is the blood:gas partition coefficient?

What does a low B/G mean? do we want B/G to be low or high?

A
  • ratio of blood conc to gas conc
  • Low B/G = low solubility = faster acting
  • want B/G to be low
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26
Q

How much is enough?

problem and solution?

A

-Partial pressure in the brain needed to block movement in response to incision
problem = we can put a probe in the brain and measure that
solution= measure partial pressure in expired gas.

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27
Q

What does 1 MAC (Min Alveolar Conc) signify?

A

1 MAC of anesthesia = amt alveolar conc at which 50% of healthy patients do not move purposefully in response to a skin incision.

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28
Q

(T/F) MAC is the same in every patient

A

F, MAC different in each patient

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29
Q

What factors decrease MAC?

A

pregnancy, age (except early age- neonate has lower MAC than an infant), infirmity

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30
Q

(T/F) Anesthesia is always titrated to effect

A

T

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31
Q

Factors that influence alveolar partial pressure during induction (how fast the patient goes under)

A
  • solubility: lower sol = faster rise
  • Conc: higher conc = faster rise
  • Alveolar ventilation: normal is optimal
  • CO: lower CO = faster rise *counterintuitive. The less blood that passes through the brain, the longer the vapor can stay there.
  • venous blood conc: higher conc = faster rise
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32
Q

Factors that influence alveolar conc during emergency (how fast the patient comes out)

A
  • Same as during induction BUT
  • Inspired conc cannot be less than zero. We cannot suck the vapor out
  • Long anesthetic time = higher venous conc; slower drop in alveolar conc (slows the emergence)
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33
Q

Physiologic effects of general anesthetics

-cellular metabolism

A

Cellular metab decreases

  • O2 consumption decr
  • Myocardial oxygen consuption decr
  • O2 demand decr
  • O2 supply decr to meatch decr demand
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34
Q

Physiologic effects of general anesthetics

-Sympathetic tone

A

Symp tone decreases

  • Arteries dilate
  • Veins dilate
  • Myocardial contractility decr
  • HR variable; some cause decr while some case reflex mediated incr
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35
Q

Physiologic effects of general anesthetics

-Direct CV effects

A
  • Decr contractility – clinical significance is variable
  • Sinus node rate changes
  • Some directly dilate arteries
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36
Q

Physiologic effects of general anesthetics

-Respiratory effects

A
  • Bronchodilation
  • Decr TV (tidal vol)-more, Incr RR (respiratory rate)-less = net result of ventrilation is decr
  • Decr response to hypercarbia
  • NO response to hypoxemia
  • CO2 apnea threshold increases
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37
Q

Physiologic effects of general anesthetics

-Effects on the brain

A
  • All functions decrease
  • Cerebral blood flow incr with halogenated agents (mismatch bw cerebral metabolic rate for O2 is decr)–concern with icreased ICP, so don’t use in intracrainial neurosurgery.
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38
Q

Physiologic effects of general anesthetics

  • Muscle
  • Kidney
  • Liver
A
  • Muscle done decr
  • GFR decr
  • Hepatic blood flow decr with CO
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39
Q

Toxicity of inhalation anesthetics:

-Renal

A

-Fluoride ions with enflurane cause renal failure

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40
Q

Toxicity of inhalation anesthetics:

-Hepatic

A
  • Metabolites of Halothane can cause hepatitis

- Don’t really see hepatic problems in children, more in adults

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41
Q

Toxicity of inhalation anesthetics:

-Respiratory

A

-Sevoflurane can make CO with CO2 absorber

but don’t really see this anymore

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42
Q

Toxicity of inhalation anesthetics:

-Malignant hyperthermia

A
  • Every anesthesiologist worries about this
  • Inherited genetically
  • Strictly a disease of anesthesia– disorder of muscle metabolism. We get hyper-metabolic state where the muscles go into contraction and rapid myolysis and extreme increase in CO2 production.
  • Caused by succinylcholine and potent inhalation anesthetics (so not NO but everything else)
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43
Q

IV anesthetics pharmacokinetics

A
  • like other drugs, effect is proportional to conc
  • rapid onset from rapid rise in conc with bolus
  • short duration from rapid redistribution
  • prolonged effect from large dose/long duration filling Vd
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44
Q

IV anesthetics pharmacodynamics

A

-same as inhaled agents: decr O2 consumption, decr CO and MAP, decr minute ventilation
BUT they decr cerebral blood flow

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45
Q

IV anesthetics pharmacodynamics are the same for that of inhalation agents except IVs decr cerebral blood flow. Which IV drug is the exception and does not decr cerebral blood flow?

A

Ketamine – it incr cerebral blood flow

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46
Q

Benzodiazepines

-What is the partial antagonist?

A
  • sedatives only (not anesthetics – though can use them to induce anesthesia but NOT to maintain it)
  • cause amnesia and unconsciousness
  • does NOT cause analgesia
  • Whats good about this class is the effects are partially antagonized by flumazenil
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47
Q

Opoids

-What drug reverses the effects of opoids?

A
  • Analgesics NOT anesthetics
  • reduce req amt of anesthetic agents
  • All effects are 100% reversible with naloxone
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48
Q

Local anesthetics

A
  • substances that cause temporary blockade of neural transmission when applied to nerve axons
  • block voltage gated Na channels –therefore interrupt nerve impulses in axons
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49
Q

Physical properties of local anesthetics

A
  • weak bases, poorly water soluble
  • synthetic – derived from cociane
  • Have hydrophilic (aromatic ring) and lipophilic end (tertiary amine) joined by an aster or amide linkage
  • Made available clinically as salts to incr solubility and stability
50
Q

Local anesthetics

-which is causes a shorter duration of action, ester linkage or amide linkage, why?

A

-Ester links bc they are more prone to hydrolysis than amide links, esters usually have a shorter duration

51
Q

Charged or uncharged form of local anesthetic causes the rxn? Why is this a problem?

A

Charged. Problem bc uncharged form is the form that can get to the site of action not the charged form.

52
Q

Mech of action of local anesthetics

A

Disruption of membrane depolarization by:

  • blocking Na conduction into cell
  • Influx of K is unchanged
  • Cellular integrity and function unchanged
53
Q

What form of the LA blocks the Na ad produces temporary dysfunction?

A

cationic form

54
Q

What does blockade of Na channel in LA mech of action req and what is it dependent on?

A
  • dep on conc

- req distribution of several contiguous channels to overcome the natural reserve of conduction in mammalian nerves

55
Q

Is the interaction of LA with the Na channel reversible? When does action end?

A
  • It is reversible

- Ends when the conc of LA falls below a critical min level

56
Q

What is differential sensitivity

A
  • Small unmyelinated fibers (B and C fibers) are more sensitive to LA
  • Large myelinated (A fibers) require larger amounts of LA to be blocked
57
Q

What is the frequency dependent block?

A

-Enhanced action of LA on a nerve which is stim or actively firing compared to nerve not firing nor active

58
Q

Why are nerves with higher firing freq and more pos membrane pot more sensitive to LA block

A

-bc the charged local anesthetic molecules are more likely to have access to the binding sites in the open Na+ channel.

59
Q

According to freq dependent block for LAs
Are fibers with a high firing rate and longer duration of AP more or less sensitive to lower concs of local anesthetics? What kind of fibers?

A
  • -More sensitive

- Sensory fibers, especially pain fibers

60
Q

Why do we need a lower conc of anesthetics to knock out pain than we do to knock out motor function?

A

Sensory fibers have longer AP duration and higher firings rate– so more sensitive to lower concs of LAs

61
Q

What fiber type is the most sensitive to LA? Type A, B or C?

A

Type-C

62
Q

What does the ester vs amide linkage in LAs determine and influence?

A
  • determines route of metabolism
  • Indirectly influences specific toxicities
  • Determines potency and duration
63
Q

What do physicochemical properties of LAs affect?

A
  • onset of action
  • potency
  • duration of action
64
Q

What is pKa?

-What is the range for most LAs? What is the exception

A

pH as which 50% of the molecules are in the charged (ionized) quaternary form and 50% are in uncharged (unionized) form.

  • Range 7.5 - 9 (weak bases) –therefore charged/ionized cationic form will be large percentage at physiological pH
    * Exception - Benzocaine has pHa of 3.5 (exists solely as nonionized base)
65
Q

Are LA solutions (vials) off the shelf acidic or basic relative to their pKa, why?

A

-acidic – to incr stability and shelf life

66
Q

What form of the LA (ionized or unionized) is necessary for nerve penetration? Ad which form delays onset of action?

A
  • Nonionized form for nerve penetration

- ionized form to delay action

67
Q

Where is the receptor site for LAs?

A

inner vestibule of the Na channel (this is deep inside the neuron)

68
Q

We need unionized form to penetrate nerve, but we want ionized for at the site of action, how does this happen?

A

-After penetration of cytoplasm (by nonionic form), equilibration leads to formation and binding of the charged cation at the Na channel

69
Q

(T/F) Potency is indirectly proportional to lipid solubility

A

F- it is directly proportional
-The cell wall is a lipid structure. Potency is really more about ability to penetrate nerve rather than at site of action

70
Q

(T/F) Duration of action is directly proportional to protein binding.
-What does protein binding also relate to?

A

T–the greater the protein binding, the longer it takes to wash out the drug.
-relates to toxicity –high protein binding reduces amt of free drug

71
Q

LA metabolism of esters

A

hydrolysis in the blood by pseudo or butyrylcholinesterase (prod in liver), or red cell esterases

72
Q

LA metabolism of amides

-What does it req?

A

-metabolized by cyt p450s (liver enzyme)– so requires intact liver

73
Q

What about the metabolism of LAs would give a prolongation of action

A

-atypical pseudocholinesterase or liver disease

74
Q

What is the absorption of LA determined by?

-How can we alter the blood flow?

A
  • dosage (how much you give them)
  • site of injection
  • drug-tissue binding
  • local tissue blood flow
  • physicochemical properties of the drug
  • alter blood flow by adding vasoconstrictor (like epi) to the LA
75
Q

LA-Rank the following in terms of absorption rate from highest (most susceptible) to lowest

  • Epidural block
  • Brachial plexus block
  • Intercostal block
  • Sciatic and Femoral nerve block
  • Caudal block
A 
1- Intercostal block (usually blocking more than one intercostal nerve so better chance to absorb it)
2- Caudal block
3- Epidural block
4- Brachial plexus block
5-Sciatic and Femoral nerve block
76
Q

(T/F) The rank of rate of absorption in each part of body (ex- intercostal) will be different depending on which drug you use.

A

F - The relationship is always the same no matter the LA drug. Some drugs might have more or less responses but the ration is the same always.

77
Q

LA toxicity:

What are the CNS initial symptoms (lower dose)?

A
  • Lightheadedness
  • Peri-oral numbness
  • Dizziness
  • Visual and Auditory disturbances (Tinnitus)
  • Disorientation
  • Drowsiness
78
Q

For LA toxicity, which signs to we see first, CNS or cardiac?

A

CNS

79
Q

LA toxicity:
What are the CNS signs with higher-doses?
When do they occur?

A
  • Muscle twitching
  • Convulsions
  • Unconsciousness
  • Coma
  • Respiratory depression and arrest
  • CV depression and collapse
  • > Often occur after initial CNS excitation followed by a rapid CNS depression
80
Q

LA toxicity:
What are the direct cardiac effects?
Which drug is especially cardiotoxic?

A
  • Myocardial depression, cardiac dysrhythmias and cardio-toxicity in pregnancy
  • Negative inotropic effects on cardiac muscle that lead to hypotension.
  • > Bupivicaine is especially cardiotoxic
81
Q

LA toxicity:

-What are the peripheral effects of low and high doses?

A

Low doses – vasconstriction

High doses – vasodilation (hypotension)

82
Q

LA toxicity:

  • What are the hematological sigs
  • What drugs cause this?
A
  • Methemoglobinemia

- Common with prilocaine and benzocaine

83
Q

What does local tissue manifestations in LAs cause?

A

-Muscle necrosis

84
Q

What are people allergic to in LAs? What is this due to?

A
  • Ester LA

- Due to para-amino benzoic acid (PABA)

85
Q

What are the treatment options of LA toxicity?

A
  • Stop injection
  • Airway, O2
  • Treat seizures with benzodiazepines
  • Cardiac: CPR, ACLS
86
Q

What is a new treatment option of LA toxicity? What does it do?

A
  • Intralipid

- It blunts the cardiotoxicity of bufiviciane

87
Q

How do we treat methemoglobinemia (LA toxicity)?

A

It’s spontaneously reversed or use Methylene Blue

88
Q

Allergic rxns in LAs usually due to? Are the common or rare?

A
  • Rare

- Due to preservatives (mathylparaben)

89
Q

How do we treat muscle tissue necrosis (LA toxicity)?

A

-spontaneously reversed in ~2 weeks

90
Q

What happens in complication of the central neuraxial block.

  • What does central mean here?
  • What happens when levels exceed T10 and Y$
  • What are the contraindication of the neuraxial blockade?
A

Central = spinal or epidural anesthesia

  • Above T10 –Knocking out 2 of 3 resevoirs –Causes profound hypotension (bc decr venous return)
  • Above T4 – Knocking out all 3 major venous resevoirs –bradycardia makes things worse (can cause cardiac arrest)
  • Contraindications: aortic stenosis, shock and coagulopathy
91
Q

Cocaine

A
  • First LA
  • Naturally occurring ester
  • High local neural toxicity
  • High abuse pot
  • Still popular topical anesthetic bc of vasoconstrictive properties
92
Q

Novocaine

A
  • Ester LA (modification of cocaine)
  • First injectable LA synthesized
  • Metabolized by pseudocholinesterase
  • Excreted by the kidneys
  • Very short acting– so unlikely to get toxicity
93
Q

Tetracaine

-Which body part is this commonly used on?

A
  • Ester LA
  • Slow onset due to high pKa
  • Long duration
  • Great topical anesthetic –> used on the eye
94
Q

What does a high pKa indicate?

A

agent is mostly ionized

95
Q

2-Chloroprocaine

A
  • Ester LA
  • Safest in terms of toxicity
  • Duration 45-60 min (short)
  • Rapid termination of effect (rapidly metabolized– why it’s safe)
  • IV – causes thrombophlebitis
96
Q

Benzocaine

A
  • First synthetic LA (ester)
  • Effective only in high conc
  • Mostly used in mucous membranes (very effective for topical, not really used for anything else.)
  • Causes methemoglobinemia
97
Q

Lidocaine

A
  • First amide LA – all others are compared to this one
  • Metabolized in liver
  • Excreted by kidneys
  • Can give IV to treat arrhythmias
98
Q

Dibucaine

A
  • Amide LA
  • High potency and toxicity
  • Inh plasma cholinesterase – used to determine if person has atypical cholinesterase
  • Only use topical as cream
99
Q

Mepivacaine

A
  • Amide LA
  • Similar to lidocaine, but less vasodilation
  • Slightly greater potency and duration
  • Use: epidural, spinal, peripheral nerve block, local infiltration
  • Potential for accumulation –> unsuitable for prolonged epidural infusion
100
Q

Bupivacaine

A
  • Amide LA
  • Greater potency and duration (can add epi for longer duration)
  • Good for spinal anesthesia
  • Slower onset
  • Several concs used
  • Sig freq dependent block
  • Has cardiotoxicity (much more than any other anesthetic)
101
Q

Ropivacaine

A
  • Amide LA
  • Almost pure S isomer (so not racemic mixture)
  • Less potent and shorter duration than Bupivacaine
  • Less cardiotoxic
  • Better freq dep block
  • Sev concs used
102
Q

Prilocaine

A
  • Amide LA (most rapidly metabolized amide LA)

- Produced methemoglobinemia

103
Q

Epi

A
  • Adjuvant to LA
  • Decreases absorptions and prolongs duration (bc vasoconstrictor– allows drug to stay in the area)
  • Also used as a monitor
104
Q

Bicarbonate

A
  • Adjuvant to LA
  • Incr pH of solution, accelerating onset
  • May decr duration
  • May precipitate in Ropivacaine and Bupivacaine (what does this mean?)
105
Q

What are 2 adjuvants for LA?

A

Epi and bicarb

106
Q

Partial pressure

A

Basic principle of anesthesiology; the tendency of an anesthetic dissolved in blood to come out of solution.

107
Q

Anesthetic effect is the result of ______ NOT ______

A

pp NOT conc

108
Q

Fentanyl

A
  • IV

- Analgesia

109
Q

Low B/G coeff

A

low solubility and faster acting

110
Q

MAC

A

That alveolar concentration at which 50% of healthy patients do not move purposefully in response to a skin incision

111
Q

Minimum alveolare conc

A

MAC

112
Q

Nitrous oxide

A

anesthetic with the highest MAC

113
Q

What is an IV effect diff from inhalation effect?

-And what drug is the exception?

A

Unlike inhaled agents, decrease cerebral blood flow (except Ketamine)

114
Q

Flumazenil

A

Partial benzodiazepine antag

115
Q

LA mech of action

-what is not affected?

A

Disruption of membrane depolarization by blocking Na+ conduction into the cell (K+ influx unchanged, cellular integrity not affected); concentration dependent

116
Q

Unmyelinated nerve fibers

A

Small (B and C) fibers appear more sensitive to local anesthetics

117
Q

Myelinated nerve fibers

A

Large A fibers require larger amounts of local anesthetic to be blocked

118
Q

What does low CO do to induction of inhaled anesthetics?

A

accelerates it

119
Q

What is duration of action proportional to?

A

Directly proportional to protein binding; also relates to toxicity - high protein binding reduces amount of free drug

120
Q

Which LA are longer acting?

A

Bupivacaine and Ropivacaine

Pharmacology Block 2 (4 decks)

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